Behavioral and neuropharmacological methods will be used to examine two notable features of organization within the limbic system. The first focus is on a set of structures recently referred to as the "extended amygdala", a system that includes the central nucleus of the amygdala, the sublenticular substantia innominata, the lateral bed nucleus of the stria terminalis and medial accumbens nucleus. The proposed work will examine the concept that this system allocates processing based on the learned significance of events. This cognitive view will be distinguished from the more traditional concept that components of this system are important for acquiring motivationally-determined associations, by which conditioned stimuli acquire either rewarding or aversive properties. Opioid peptide function in the extended amygdala will be examined within this framework. The second focus is on a system of prominent projections from the hippocampal formation and basolateral complex of the amygdala (ABL) that innervate the extended amygdala. Damage to either the hippocampal formation or ABL spares simple associative teaming, but these limbic structures are critical for more complex associative processes that can be studied in classical conditioning paradigms. The ABL will serve as a focus for examining its role in cross modal sensory/sensory associations and for determining the contribution of a N-methyl-D-aspartate mechanism to this form of learning. Then experiments are proposed to determine whether specific associative processes, that are dependent on the ABL and hippocampal formation, are implemented by their projections to the extended amygdala. These experiments are based on a model by which limbic inputs to the extended amygdala are gated by dopaminergic innervation from the ventral tegmentum. We will determine whether neurotoxic lesions that remove limbic inputs result in a selective loss of D2 binding in the extended amygdala. Then we will assess whether D2, but not D1, agonists microinjected into the extended amygdala selectively disrupt associative processes that depend on the integrity of the hippocampal formation and the ABL.